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. 2018 Aug 27;14:1744806918795930. doi: 10.1177/1744806918795930

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© The Author(s) 2018

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 7. — Schematic representation of the potential mechanisms by which the P2X4 receptor in activated microglia modulates EAAT3 expression in the TNC in an IS-induced trigeminal allodynia model. Following repeated dural inflammatory stimulation, P2X4R expression is elevated in TNC microglia. Upregulation of microglial P2X4R promotes the activation of p38-MAPK and the synthesis and release of BDNF. By acting on its high-affinity receptor, TrkB, BDNF upregulates the glutamate transporter EAAT3. Glutamate influx through EAAT3 may further activate intracellular metabotropic glutamate 5 receptor (mGluR5), which is essential for enhanced Ca²⁺-dependent Fos and plays a crucial role in the glutamate-induced neuroplasticity underlying persistent pain.^12,46–50

EAAT3: excitatory amino acid transporter 3; TrkB: tyrosine receptor kinase B; P2X4R: P2X4 purinoceptor; BDNF: brain-derived neurotrophic factor.